Anurag Goel ST5, Gastroenterology. Definition: presence of free - - PowerPoint PPT Presentation
Anurag Goel ST5, Gastroenterology. Definition: presence of free - - PowerPoint PPT Presentation
Anurag Goel ST5, Gastroenterology. Definition: presence of free fluid in the peritoneal cavity Caus uses es of of Asc scites ites Cause Frequ quency ncy Cirrhosis 81% Cancer 10% Heart Failure 3% Tuberculosis 2% Dialysis
Definition:
presence of free fluid in the peritoneal cavity
Cause Frequ quency ncy Cirrhosis 81% Cancer 10% Heart Failure 3% Tuberculosis 2% Dialysis 1% Pancreatic Disease 1% Other 2%
Caus uses es of
- f Asc
scites ites
Non-peritoneal causes Examples
Intrahepatic portal hypertension Cirrhosis Fulminant hepatic failure Veno-occlusive disease Extrahepatic portal hypertension Hepatic vein obstruction (ie, Budd-Chiari syndrome) Congestive heart failure Hypoalbuminemia Nephrotic syndrome Protein-losing enteropathy Malnutrition Miscellaneous disorders Myxedema Ovarian tumors Pancreatic & Biliary ascites Chylous Secondary to malignancy, trauma
Peritoneal Causes Examples
Malignant ascites Primary peritoneal mesothelioma Secondary peritoneal carcinomatosis Granulomatous peritonitis Tuberculous peritonitis Fungal and parasitic infections Sarcoidosis Foreign bodies (cotton ,starch, barium) Vasculitis Systemic lupus erythematosus Henoch-Schönlein purpura Miscellaneous disorders Eosinophilic gastroenteritis Whipple disease Endometriosis
Catego gory ry
Infectious diseases Amebiasis, Ascariasis, Brucellosis, Chlamydia peritonitis, Complications related to HIV infection, Pelvic inflammatory disease, Pseudomembranous colitis, Salmonellosis, Whipple's disease Hematologic Amyloidosis, Castleman's syndrome, Extramedullary hematopoiesis, Hemophagocytic syndrome, Histiocytosis X, Leukemia, Lymphoma, Mastocytosis, Multiple myeloma Miscellaneous Abdominal pregnancy, Crohn's disease, Endometriosis, Gaucher's disease, Lymphangioleiomyomatosis, Myxedema, Nephrotic syndrome, lymphatic tear or ureteral injury. Ovarian hyperstimulation
Ultrasound with Dopplers
- Easily confirms ascites
- May see nodularity of cirrhosis
- Evaluate patency of vasculature
- No radiation, contrast
CT / MRI
- Evaluation for malignancy
Grade 1
- Mild, only detectable by U/S
Grade 2
- Moderate, symmetrical distension
Grade 3
- Gross or large with marked distension
Large typically means painful/uncomfortable
Refractory Ascites (5-10%)
- Can not be mobilized or early recurrence
refractory to medical management
NEJM 350:1646-54 Hepatology 2003; 38: 258-266
15cm lateral and 2 cms below umbilicus Avoid enlarged spleen and liver Avoid sp and inf epigastric arteries No data to support use of FFP Most clinicians would give pooled platelets
if <40
Complication:
- Haematoma<1%
- Bowel perforation/haemoperitoneum <0.1%
10-20ml of fluid in a syringe with
blue/green needle
Go 2cm below the umbilicus in the midline or 3 cm superior and medial to the anterior superior iliac spine
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Routi tine ne Optional nal Unusual Cell count and differential Glucose concentration Tuberculosis smear and culture, adenosine deaminase Albumin concentration LDH concentration Cytology Total protein concentration Gram stain Triglyceride concentration Culture in blood culture bottles Amylase concentration Bilirubin concentration
Is portal hypertension present? 97% accurate
SAAG > 11 g/L Portal HTN SAAG < 11 g/L Other causes SAAG = (albumin concentration of serum) - (albumin concentration of ascitic fluid)
The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Runyon BA; Montano AA; Akriviadis EA; Antillon MR; Irving MA; McHutchison Ann Intern Med 1992 Aug 1;117(3):215-20.
SAAG > 1 11 g/L (PORTAL RTAL HT) SAAG < 1 11 g/L Cirrhosis Peritoneal carcinomatosis Alcoholic hepatitis Peritoneal tuberculosis CHF Pancreatitis Massive hepatic metastases Serositis Budd Chiari Syndrome Nephrotic syndrome Congestive heart failure/constrictive pericarditis
SAAG > 11 SAAG < 11
Ascites Protein <25 Ascites Protein >25
- 1. Check serum
and fluid albumin
Ascites Protein >25
- 2. Check Ascites
Protein
Hepatic Sinusoid source Peritoneum source Capillarized sinusoid Normal sinusoid Peritoneal lymph
Cirrhosis Late Budd-Chiari
- 3. Differential
Diagnosis
Cardiac ascites Early Budd-Chiari Veno-occlusive disease Malignancy Tuberculosis
The SAAG does not need to be repeated after the initial measurement.
Note: Exceptions exist: may have mixed features
Adapted from www.gastro.org
Is ascites infected?
- Greater than 250 PMN = SBP
If ascites is bloody ( > 50,000 RBC/mm3), correct by subtracting 1 PMN / 250 RBC
Is ascites bloody?
- 5% of pts w/ cirrhosis - spontaneous or s/p
traumatic tap.
Non-traumatic associated with malignancy
- 20% of malignant ascites
- 10% of peritoneal carcinomatosis
- Total protein >10 g/L
- Glucose <2.8 mmol/L
- LDH greater than serum ULN
- Low sensitivity + specificity however.
Consistent with infection or malignancy?
- Infection and cancer consume glucoselow
LDH is a larger molecule than glucose, enters
ascitic fluid with difficulty.
- Ascitis/Serum LDH ratio
~ 0.4 in cirrhotic ascites Approaches 1.0 in SBP >1.0, usually infection or tumor
Amylase
- Uncomplicated cirrhotic ascites
About 40 IU/L. The AF/S ratio is about 0.4
- Pancreatic ascites
About 2000 IU/L. The AF/S ratio is about 6
Triglycerides — milky fluid.
- Chylous ascites - TG > 200 mg/dL, usually 1000
mg/dL
Bilirubin — brown ascites.
- Biliary perforation – AF Bili > serum Bili
Smear – extremely insensitive Culture – 62-83% when large volumes
cultured
Cell count – mononuclear cell predominance Adenosine deaminase –
- Enzyme involved in lymphoid maturation
- Falsely low in pts with both cirrhosis and TB
“almost 100%” with peritoneal carcinomatosis
have positive cytology
Malignant ascites from massive hepatic mets,
HCC, lymphoma are usually negative
Overall sensitivity for detection of
malignancy-related ascites is 58 to 75 %
pH
pH,
lactate
te,
‘humoral tests of malignancy’ such as
fibronecti ronectin, cholest ester erol. l.
No clinical data to back up the finding that
upright position is asscociated with reduced GFR and reduced Na excretion and reduced diuretic efficacy
Bed rest promote muscle atrophy and other
complications and extends hospital stay
So bed rest not recommended
Typical UK diet has 150mmol/day- 15%
added salt and 70% is manufactured salt
Suggestion is no added salt diet and
avoidance of prepared food
So that patient gets 90mmol/day ( 5.2gm) Lowers diuretic requirement, faster
resolution of ascites and shorter hospital stay
Avoid high salt content of fluid and
medicine except in HRS
No role in uncomplicated ascites Most hepatologists restrict fluid in ascites associated with
hyponatraemia- but is illogical
The downside is water restriction causes increase in the
central effective hypovolaemia- more ADH- more water retension and further dilutional hyponatraemia
So hepatologist including the authors of the BSG guidelines
suggest further plasma expansion to inhibit ADH secretion
Data emerging supporting use of specific vasopressin 2
receptor antagonists
To be effective the intake should be less than urine output
rather than arbitrary 1.5L/day
If the serum sodium concentration does not increase within
the first 24 to 48 hours, the degree of fluid restriction has been insufficient.
Spironolactone is drug of choice Aldosterone antagonist acting in distal
tubule to increase natriuresis and conserve potassium
Initial dose 100mg and increasing up to
400mg
Lag of 3-5days Better natriuresis and diuresis than a loop
diuretic
Antiandrogenic effect- gynaecomazia-
tamoxifen 20mg bd
Hyperkalaemia frequently limits the use
Frusemide has low efficacy in cirrhosis Use only if 400mg of spironolactone fails to
achieve weight loss
Start at 40mg a day and increasing by 40mg
every 3rd day to max of 160mg
Watch out for metabolic alkalosis and
electrolyte disturbance
Weight loss
- Loose 0.5kg a day when no edema
- Loose 1kg a day when edema is
present
Avoid renal failure Response rate in up to 90%
patients who do NOT have renal dysfunction
Hepatology 2003; 38: 258-266 Dig Dis 2005; 23:30-38
Over diuresis is associated with
intravascular volume depletion, leading to renal impairment, hepatic encephalopathy and hyponatraemia
10% will have refractory ascites Dietary history to exclude salt ingestion-
24hr urinary Na excretion should be less than recommended intake
Drug history - NSAID
Na 126-135 and normal creatinine Continue diuretic Do not water restrict Na 121-125 and normal creatinine Continue/? discontinue Na 121-125 and high Creatinine Stop diuretic and give volume expansion Na <120 Stop diuretic
Give only if renal function is worsening –
creatinine >150 or 120 and rising
Gelofusion/Haemaccel/ 4.5% albumin –all
have 153mmol of Na per L
This will worsen salt retention but better to
have ascites than to develop HRS
Re
Refractory ctory asci cite tes- cannot be mobilised or early recurrence of which ( that is after therapeutic paracentesis) cannot be prevented by medical treatment
Diuretic
etic resista stant nt asci cite tes- refractory to dietary salt restriction and intensive diuretic treatment ( spironolactone 400mg and frusemide 160mg per day and salt restricted diet of less than 90mmol/day ( 5.2g/day)
Diuretic
etic intol
- lerant
erant as asci cite tes- refractory to therapy due to the development of diuretic induced complications
Total paracentesis is associated with
significant haemodynamic changes
Large volume paracentesis causes marked
reduction of IAP and IVC pressure- decrease in right heart pressure and
This changes are maximal at 3hrs
International ascites club recommend if <5L is removed
synthetic plasma expander can be used and as good as albumin ( some hepatologist suggests no albumin/plasma expander if <5L)
Compared to albumin, artificial plasma expander cause more
activation of Rennin Angiotensin System , causes more hyponatraemia and results in longer hospital stay
20% albumin should be infused after paracentesis of >5L at
dose of 8g/L of ascites drained ( 100ml of 20% albumin= 20gm, so 3L of ascites fluid removal needs 3x8=24 gm of albumin replacement = 125ml but we tend to round it to 100ml)
5 percent albumin can be given if dehydration is suspected.
Use Z technique- puncture site on the skin
does not overlie the puncture site on peritoneum
Left flank is preferrable to right flank After drain is out patient lie on opposite site Colostomy bag if continuous leakage (
some use purse string suture)
As rapidly as possible- should not be left
- vernight
No upper limit of 8 litres or maximum time
- f 6 hours has been mentioned in the
guidelines
Transjugular
Intrahepatic Portosystemic Shunt
Creates a conduit
from the high pressure portal system to the lower pressure systemic circulation
Highly effective treatment Complete resolution in 75% of cases No effect on survival in one study and reduced on
- thers- compared with therapeutic paracentesis
HE occurs in 25% of patients , more if >60yrs May precipitate heart failure as increase cardiac
preload
TIPSS should be considered for patients who
require frequent paracentesis ( >3 a month)
It also shown to resolve hepatic hydrothorax in 60-
70%
MELD was originally developed to predict survival
after TIPSS insertion
Mortality of 50% within 2yr of diagnosis Once refractory to medical therapy 50% die
within 6 months
Time for referral to transplant centre as
paracentesis and TIPSS does not improve long term survival except improving quality of life
Spontaneous Bacterial Peritonitis
Initiate for PMN≥250/mm3 Antibiotic – follow trust guidelines Duration of therapy unclear
- 2 weeks suggested if Blood
cultures(+)
- If repeat paracentesis at 48 hours
shows PMN≤250/mm3, then 5-7 days of treatment may be adequate
40% develop HRS during the course of
illness.
Human Albumin 1.5gm/Kg o day one and
1 gm/Kg on day three has shown improvement in both morbidity and mortality. Ult ltim imat ate e treatme ment: nt: Liver transplant.
70 % recurrence in 1 yr
Prophylactic antibiotics should
also be prescribed indefinitely unti til l ascite ites has elimina iminated ted
Options include:
- Bactrim DS 1 tab po 5 days/week
- Cipro 750mg po q week
1.
Up to Date
2.
Ascites and renal dysfunction in liver disease, Second edition. Edited by Pere Ginès, Vicente Arroyo, Juan Rodés, and Robert W. Schrier. Malden, Mass., Blackwell, 2005.
3.
The serum-ascites albumin gradient is superior to the exudate- transudate concept in the differential diagnosis of ascites. Runyon BA; Montano AA; Akriviadis EA; Antillon MR; Irving MA; McHutchison Ann Intern Med 1992 Aug 1;117(3):215-20.
4.
Becker, G. Malignant ascites: Systematic review and guideline for
- treatment. European Journal of Cancer 42 (2006) 589 - 597
5.
Aslam, N. Malignant ascites; New concepts in pathophysiology, diagnosis, and management. Arch Intern Med. Vol 161. Dec 10/24, 2001.
Cause Testi ting ng Alcoholic liver disease History, AST / ALT > 2 Chronic hepatitis C Hep C Ab, Viral load Primary biliary cirrhosis Antimitochondrial antibodies Primary sclerosing cholangitis Contrast cholangiography , ANA, Anti smooth muscle Ab, ANCA Autoimmune hepatitis Type 1: ANA, ANCA antismooth muscle Ab Type 2: anti-LKM-1 Chronic hepatitis B Hepatitis B serologies Hemochromatosis Ferritin, genetic testing Wilson’s disease Ceruloplasmin Alpha-1-antitrypsin deficiency Serum AAT Nonalcoholic fatty liver disease Hx of DM or metabolic syndrome
Occur when weight of
ascites is sufficient to push the flanks
- utwards
Difficult to
distinguish from
- besity
Sensitivity-72-93%
- Pooled data 81%
Specificity-44-70%
- Pooled data 59%
JAMA 1992; 267:2645-48
Similar to bulging
flanks, although uses percussion
Typically bowel will
float to the top and ascitic fluid sinks to the bottom
Sensitiv
itivity ity-80 80-94% 94%
- Most sensitive test
- Pooled data 84%
Specificity-29-69%
- 69% outlying value
- Pooled data 59%
JAMA 1992; 267:2645-48
Find the point where
flank dullness occurs
Mark it Roll the patient away
from the examiner
Repeat percussion
and ensure that the point moves to the dependent side
Sensitivity-60-83%
- Pooled data 77%
Specificity-56-90%
- Pooled data 72%
JAMA 1992; 267:2645-48
Medial edges of both
hands down midline
Tap flank firmly and
feel for an impulse on the other side
Sensitivity-50-80%
- Pooled data 62%
Spec
ecifi ificity city-82 82-92% 92%
- Most specific test
- Pooled data 90%
JAMA 1992; 267:2645-48
Have patient prone 3-5
minutes then rise to crawling
Place the diaphragm of
the stethoscope over the most dependent area of the abdomen
Flick a finger until sound
detected
No longe
nger recommended ended
Formerly used for high
sensitivity
Sensitivity-43-55%
- Pooled data 45%
Specificity-51-83%
- Pooled data 73%
JAMA 1992; 267:2645-48
Ultrasound is the
most sensitive test for ascites (100mL detection)
- Have to use caution as
small or even moderate ascites may be difficult to tap (even when marked)
- Ensure mark is
appropriate
Go with patient to U/S (ideal) If not possible, in order specify location where you want to place your needle
Image from www.gastro.org
Definition: abnormal accumulation of fluid
in the peritoneal cavity as a consequence of cancer.
Commonly caused by cancers of:
- Breast, bronchus, ovary, stomach, pancreas, colon
20% of cases have tumors of unknown
primary
Survival poor – usually less than 3 months Becker, G. Malignant ascites: Systematic review and guideline for treatment. European Journal of Cancer 42 (2006) 589 - 597
Obstruction of lymphatics by tumor
- Prevents absorption of fluid and protein
Alteration in vascular permeability
- Hormonal mechanisms (VEGF, IL2, TNF alpha)
Decreased circulating blood volume
- Activates RAAS leading to Na retention
Becker, G. Malignant ascites: Systematic review and guideline for treatment. European Journal of Cancer 42 (2006) 589 - 597
Denver Shunt (Similar to LaVeen Shunt)
Contraindications
- Protein > 4.5 g/l (occlusion)
- Loculated ascites
- Coagulopathy
- Advanced renal/cardiac disease
- GI malignancy
Complications
- Infection
- Hematogenous spread of mets
- DIC
- Pulmonary edema
- Pulmonary emboli
Therapeutic paracentesis
- Removing up to 5L appears safe
- No good data on role of volume expanders
Diuretics
- Equivocal evidence of efficacy
- May be helpful for portal HTN
- Less/minimally useful when no portal HTN
Drainage Catheters Peritoneovenous shunts